Thyrotropin-releasing hormone (TRH)-induced facilitation of spinal neurotransmission: a role for NMDA receptors.

Thyrotropin-releasing hormone (TRH) is known to enhance spinal reflexes and modulate NMDA receptors in supraspinal areas. We have investigated the relationship between TRH and NMDA receptors in the spinal cord of alpha-chloralose-anaesthetized spinalized rats. TRH was tested (a) on dorsal horn neurone responses to iontophoretic NMDA, AMPA and kainate and (b) on spinal reflexes evoked by noxious pinch and electrical stimulation (2 Hz) shown to involve NMDA receptor activation. TRH given i.v. (0.5 mg/kg) or iontophoretically selectively potentiated neuronal responses to NMDA. TRH (0.5-2 mg/kg) also dose-dependently increased single motor unit reflex responses. The NMDA antagonist ketamine (2 mg/kg i.v.) abolished these TRH effects; ketamine reduced single motor unit (SMU) reflex responses more effectively when administered after TRH than in pre-TRH control tests. These results indicate that TRH-induced facilitation of spinal sensory transmission involves NMDA receptor activation.